Evidence map›Paper›PMID 29946322›Full record

ArticleFrontiers in immunology2018

The Transcription Factor NFATc1 Supports the Rejection of Heterotopic Heart Allografts.

Johannes Baur, Christoph Otto, Ulrich Steger, Stefan Klein-Hessling, Khalid Muhammad, Tobias Pusch, Krisna Murti, Rhoda Wismer, Christoph-Thomas Germer, Ingo Klein and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 47% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. NFATc1 Abrogation in B Cells Ameliorates Contact Hypersensitivity Responses.International journal of molecular sciences · 2025
    Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Johannes BaurDepartment of General, Visceral, Vascular, and Pediatric Surgery, University Hospital of Würzburg, Würzburg, Germany.
Christoph OttoExperimental Surgery, Department of General, Visceral, Vascular, and Pediatric Surgery, University Hospital of Würzburg, Würzburg, Germany.
Ulrich StegerDepartment of General, Visceral, Vascular, and Pediatric Surgery, University Hospital of Würzburg, Würzburg, Germany.
Stefan Klein-HesslingDepartment of Molecular Pathology, Institute of Pathology, Comprehensive Cancer Center Mainfranken, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Khalid MuhammadDepartment of Molecular Pathology, Institute of Pathology, Comprehensive Cancer Center Mainfranken, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Tobias PuschDepartment of Molecular Pathology, Institute of Pathology, Comprehensive Cancer Center Mainfranken, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Krisna MurtiDepartment of Molecular Pathology, Institute of Pathology, Comprehensive Cancer Center Mainfranken, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Rhoda WismerDepartment of Molecular Pathology, Institute of Pathology, Comprehensive Cancer Center Mainfranken, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Christoph-Thomas GermerDepartment of General, Visceral, Vascular, and Pediatric Surgery, University Hospital of Würzburg, Würzburg, Germany.
Ingo KleinTransplant and Hepatobiliary Surgery, Department of General, Visceral, Vascular, and Pediatric Surgery, University Hospital of Würzburg, Würzburg, Germany.
Nora MüllerInstitute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany.
Edgar SerflingDepartment of Molecular Pathology, Institute of Pathology, Comprehensive Cancer Center Mainfranken, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Andris AvotsDepartment of Molecular Pathology, Institute of Pathology, Comprehensive Cancer Center Mainfranken, Julius-Maximilians University of Würzburg, Würzburg, Germany.
Universitätsklinikum Würzburg · DEComprehensive Cancer Center Mainfranken · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune suppressants cyclosporin A (CsA) and tacrolimus (FK506) are used worldwide in transplantation medicine to suppress graft rejection. Both CsA and FK506 inhibit the phosphatase calcineurin (CN) whose activity controls the immune receptor-mediated activation of lymphocytes. Downstream targets of CN in lymphocytes are the nuclear factors of activated T cells (NFATs). We show here that the activity of NFATc1, the most prominent NFAT factor in activated lymphocytes supports the acute rejection of heterotopic heart allografts. While ablation of NFATc1 in T cells prevented graft rejection, ectopic expression of inducible NFATc1/αA isoform led to rejection of heart allografts in recipient mice. Acceptance of transplanted hearts in mice bearing NFATc1-deficient T cells was accompanied by a reduction in number and cytotoxicity of graft infiltrating cells. In CD8

Indexed as

CD8+ T cellsChIPseqheterologousmetabolismNFATc1transplantation

Identifiers

PMID29946322
PMCPMC6005848
OpenAlexW2806466758

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.